Chitosan polymer sizes effective in inducing phytoalexin accumulation and fungal suppression are verified with synthesized oligomers.

Biologically derived chitosan has been reported to induce pisatin and disease resistance response proteins in pea tissue and also to inhibit the germination and growth of some fungal pathogens. Stereo-controlled synthesis of chitosan tetramer, hexamer, and octamer allowed the precise verification of oligomer size required for biological activity. The octameric oligomer optimally induced pisatin accumulation and inhibited fungal growth, verifying previous results obtained with column-purified oligomers derived from crab shells.

An experimental study of the acute stage of subarachnoid hemorrhage.

A baboon model of subarachnoid hemorrhage (SAH) has been developed to study the changes in cerebral blood flow (CBF), intracranial pressure (ICP), and cerebral edema associated with the acute stage of SAH. In this model, hemorrhage was caused by avulsion of the posterior communicating artery via a periorbital approach, with the orbit sealed and ICP restored to normal before SAH was produced. Local CBF was measured in six sites in the two hemispheres, and ICP monitored by an implanted extradural transducer. Following sacrifice of the animal, the effect of the induced SAH on ICP, CBF, autoregulation, and CO2 reactivity in the two hemispheres was assessed. Brain water measurements were also made in areas of gray and white matter corresponding to areas of blood flow measurements, and also in the deep nuclei. Two principal patterns of ICP change were found following SAH; one group of animals showed a return to baseline ICP quite quickly and the other maintained high ICP for over an hour. The CBF was reduced after SAH to nearly 20% of control values in all areas, and all areas showed impaired autoregulation. Variable changes in CO2 reactivity were evident, but on the side of the hemorrhage CO2 reactivity was predominantly reduced. Differential increase in pressure lasting for over 7 minutes was evident soon after SAH on the side of the ruptured vessel. There was a significant increase of water in all areas, and in cortex and deep nuclei as compared to control animals.

Dural arteriovenous malformations of the spine. Clinical features and surgical results in 55 cases.

The clinical and angiographic findings of 55 patients with a spinal dural arteriovenous malformation (AVM) are reviewed, and the results of surgery assessed. The symptoms of dural AVM are usually gradual in onset, and hemorrhage from this type of AVM is less common than in true spinal cord angiomas. Other clinical features and the myelographic findings are similar to those of spinal cord angiomas. On angiography, the nidus of dural AVM's usually projected lateral to the spinal cord. Clipping of communicating vessels between the AVM and the coronal plexus was carried out in 50 patients, and decompressive laminectomy only in five cases. Surgery led to improvement of disturbed gait or arrest of a previously progressive course in 85% of those managed by clipping communicating vessels. The pathophysiology and surgical treatment of dural AVM's are discussed.

Effect of stimulation of the medullary reticular formation on cerebral vasomotor tonus and intracranial pressure.

The authors report the results of a study to evaluate the effect of stimulation of the medullary reticular formation on cerebral vasomotor tonus and intracranial pressure (ICP) after the hypothalamic dorsomedial nucleus and midbrain reticular formation were destroyed. Systemic arterial pressure (BP), ICP, and local cerebral blood volume (CBV) were continuously recorded in 32 cats. To assess the changes in the cerebral vasomotor tonus, the vasomotor index defined by the increase in ICP per unit change in BP was calculated. In 29 of the 32 animals, BP, ICP, and CBV increased simultaneously immediately after stimulation. The increase in ICP was not secondary to the increase in BP, because the vasomotor index during stimulation was significantly higher than the vasomotor index after administration of angiotensin II. The vasomotor index was high during stimulation of the area around the nucleus reticularis parvocellularis. In animals with the spinal cord transected at the C-2 vertebral level, ICP increased without a change in BP. These findings indicate that the areas stimulated in the medullary reticular formation play an important role in decreasing cerebral vasomotor tonus. This effect was not influenced by bilateral superior cervical ganglionectomy, indicating that there is an intrinsic neural pathway that regulates cerebral vasomotor tonus directly. In three animals, marked biphasic or progressive increases in ICP up to 100 mm Hg were evoked by stimulation. The reduction of cerebral vasomotor tonus and concomitant vasopressor response induced by stimulation of the medullary reticular formation may be one of the causes of acute brain swelling.

Hemifacial spasm caused by a spontaneous dissecting aneurysm of the vertebral artery. Case report.

The authors describe the first reported case of dissecting aneurysm presenting with hemifacial spasm. The patient was a 58-year-old woman with left hemifacial spasm of 2 years' duration. Cranial nerve examination was otherwise normal and no other clinical symptoms were observed. Vertebral angiography revealed a fusiform enlargement of the left vertebral artery and contrast medium remaining in the intramural false lumen in the venous phase. Microvascular decompression of the facial nerve with wrapping of the aneurysm resulted in complete relief of the hemifacial spasm.

Artificial embolization with isobutyl-2-cyanoacrylate for the treatment of carotid-ophthalmic aneurysm.

A large carotid-ophthalmic aneurysm was successfully obliterated by the combined treatment of clipping the aneurysmal neck and intraaneurysmal injection of isobutyl-2-cyanoacrylate. Reflux of the glue into the artery was prevented by temporary trapping of the carotid artery. The obliteration of an aneurysm with isobutyl-2-cyanoacrylate is an effective procedure in cases where clipping of the aneurysmal neck is not completed due to technical difficulties.

A comparison of intraarterial carboplatin and ACNU for the treatment of gliomas.

BACKGROUND: Intraarterial chemotherapy with carboplatin for malignant gliomas has been tried recently, but its therapeutic efficacy and toxicity have not yet been elucidated. METHODS: We treated patients with malignant glioma by intraarterial chemotherapy using carboplatin, and compared the efficacy as well as the side effects with intraarterial ACNU. RESULTS: Twenty patients were treated with carboplatin (300 mg/m2) and 22 patients were treated with ACNU (80-200 mg/m2). Response (complete remission+partial response) rate for carboplatin was 12.5% compared to 45% for ACNU. Despite higher response rate for ACNU, the difference in the survival curves of the two groups was not significant. Three patients who were treated with high dose (150-200 mg/m2) of ACNU developed hemiparesis and aphasia. Seven patients treated with carboplatin developed 10 incidences of neurotoxicities; two hemiparesis, one aphasia, one blindness, one visual field disturbance, three convulsions, and two developed incidences of disturbances of consciousness. CONCLUSIONS: Intraarterial carboplatin was not superior to intraarterial ACNU in achieving remissions, and showed much greater tendency to produce neurotoxicities.

Prediction and evaluation of brainstem function by auditory brainstem responses in patients with uncal herniation.

Serial measurements of auditory brainstem-evoked responses (BERs) were conducted in 15 patients with supratentorial mass lesions. Significant prolongation of the latency of wave V BERs, which originates in the inferior colliculus, occurred when the intracranial pressure (ICP) approached 30 mmHg. In four of five patients whose BERs were measured before pupillary changes, a significant lengthening of wave V latency was observed prior to clinical manifestation of uncal herniation. These results suggest that immediate medical or surgical decompression of ICP should be performed when ICP approaches 30 mmHg with significant prolongation of wave V latency.

OPC-21268, an orally effective, nonpeptide arginine vasopressin V1 receptor antagonist reduces vasogenic brain edema.

We examined the effect of orally administered OPC-21268, a nonpeptide Arginine Vasopressin V1 receptor antagonist, on cold induced vasogenic brain edema in rat. Cold brain injury was induced by applying a copper rode cooled with liquid nitrogen for one minute. To mimic clinical use, one hour after induction of the cold lesion, rats were treated with orally administered OPC-21268 at doses of 100 mg, 200 mg, and 300 mg/kg every 8 hr for 24 hours. Two percent Evans blue in saline, in a volume of 1 ml/kg was given intravenously prior to cold injury. Twenty four hours after induction the cold lesion, brain water, brain tissue electrolytes, and plasma osmolality and electrolytes were measured. Quantitative evaluation of BBB permeability was performed using the Evans blue fluorescence method. The injury resulted in significant increases in the brain water and brain tissue sodium, and Evans blue concentration in both the lesioned and contralateral hemispheres (p < 0.01). OPC-21268 at doses of 200 mg and 300 mg/kg significantly decreased brain water and Evans blue concentrations in both the lesioned and contralateral hemispheres (p < 0.01). Brain tissue sodium content was significantly reduced at a dose of 300 mg/kg in the lesioned side (p < 0.05). There were no significant changes in other parameters throughout the experiments. Our results indicate that OPC-21268 exerts a protective effect in areas where the maximal amount of BBB breakdown occurs.

Treatment of acute intracranial hypertension with RU 51599, a selective kappa opioid agonist.

RU 51599, a selective kappa opioid agonist which is a potent aquaretic, was studied for its effect on acute intracranial hypertension. In ketamine anesthetized cats acute intracranial hypertension was induced by progressive inflation of an epidural balloon with physiological saline at a constant rate of 0.5 ml/hr for three hours. In the control group (n = 8), the balloon was maintained inflated for another an hour after which it was deflated. In the post deflation period monitoring was continued for one hour. In the treatment group (n = 8), cats were treated by an intravenous (i.v.) injection of RU 51599, at a dose of 1 mg/kg every hour at the beginning of balloon inflation, during balloon inflation, at the completion of inflation, and after deflation. Changes in intracranial pressure (ICP), mean arterial blood pressure (MAP), cerebral perfusion pressure (CPP), blood gases, serum electrolytes and osmolality, and brain water content water content were studied in both groups. In the control group, epidural brain compression resulted in significant increases in the mean ICP up to 80.7 +/- 9.8 mmHg at 3 hrs (during balloon inflation), 68.6 +/- 8.3 after complete inflation, and 62.1 +/- 11.4 mmHg after deflation (P < 0.01), and significant decreases in CPP to 55.5 +/- 14.0 mmHg at 3 hrs (during balloon inflation), 43.0 +/- 11.2 mmHg after inflation, and 36.3 +/- 9.9 mmHg after deflation (P < 0.01). In the treatment group there were significant decreases in the mean ICP to 35.2 +/- 6.8 mmHg at 3 hrs (during balloon inflation), 32.3 +/- 7.9 after inflation, and 16.1 +/- 3.6 mmHg after deflation (P < 0.01), and significant increases in CPP to 103.2 +/- 6.1 mmHg at 3 hrs (during balloon inflation), 109.0 +/- 8.8 mmHg after inflation, and 102.7 +/- 8.2 mmHg after deflation (P < 0.01). Brain water content was also significantly reduced (P < 0.05). There were no significant changes in the serum electrolytes and osmolality throughout the experiments. Our results suggest that, the mechanism by which RU 51599 reduces ICP is related to reduction in the brain water content.

Significance of multimodal cerebral monitoring under moderate therapeutic hypothermia for severe head injury.

The therapeutic significance of moderate hypothermia and cerebral monitorings was assessed in the 10 patients with severe head injury. Cooling was begun as soon as possible after admission, using water blankets under general anesthesia. Jugular venous or tympanic temperature of patients was maintained at 32 degrees C for 3 to 5 days, then rewarming at the rate of 1 degree C a day was started. The intracranial pressure was controllable less than 20 mmHg under hypothermia. Moderate hypothermia reduced the jugular venous lactate (33.5%) as well as the cerebral blood flow velocity at M1 portion of middle cerebral artery (CBFV-M1) measured by transcranial Doppler (7.2%), while increase of the jugular venous oxygen saturation (SjO2) (17.9%) was observed in a majority of the patients. Our results demonstrated that moderate therapeutic hypothermia significantly reduced cerebral circulation and metabolism. Measurement of SjO2 and CBFV-M1 seems to be useful for estimation of cerebral circulation and metabolism in therapeutic hypothermia.

Sequential changes in MR images of the brain in acute carbon monoxide poisoning.

Two cases of acute carbon monoxide poisoning are presented in this paper. Sequential magnetic resonance (MR) images of the brain showed abnormal lesions in the bilateral globus pallidus and/or in the subcortical white matter. The MR images disclosed that the severity of the white matter lesions correlated with the prognosis in acute carbon monoxide poisoning. However, they did not always correspond to the neurological condition in the acute and subacute stages.

Spinal cord hemangioblastoma presenting with subarachnoid hemorrhage.

A 41-year-old man presented with subarachnoid hemorrhage (SAH) caused by a cervical spinal cord hemangioblastoma. There were no features to distinguish the SAH from that due to an intracranial lesion. The diagnosis was established by cerebral angiography, computed tomography, and magnetic resonance imaging. The tumor was located in the right dorsolateral aspect of the cervical spinal cord. Hemilaminectomy was performed, and the tumor was completely removed. No postoperative neurological deficit was observed. The possibility of a spinal origin for SAH should be considered if no cranial origin can be detected.

[Treatment of spinal cord arteriovenous malformation by surgical excision combined with afferent vessel coagulation-report of a case (author's transl)].

A case of spinal cord arteriovenous malformation was reported, in whom serial selective spinal angiogram and pantopaque myelogram showed a successful demonstration of intramedullary nidus. A 25-year-old male was admitted with paraparesis, impotence, hypesthesia and hypalgesia in his legs in 1974. He was diagnosed to have a spinal cord arteriovenous malformation of so-called "glomus type" with intramedullary nidus by the selective spinal angiogram and pantopaque myelogram. The nidus was fed by the anterior spinal artery through the 8th intercostal artery, from which a major draining vein extended caudally, but there was also some cranial drainage. The arteriovenous malformation was treated by surgical excision combined with afferent vessels coagulation in order to prevent the rupture of the remaining intramedullary nidus. After operation the patient develop a transient analgesia and girdle pain at T9-10 level, but after 42 days he regained full muscle power in his legs and could run by himself, while sensory disturbance remained about the same as before surgery.

[Evaluation of the role of brain scintigraphy in pineal tumors (author's transl)].

From January, 1969 to December, 1975, 1700 patients underwent sequential brain scintigraphy with Tc-99-m-pertechnetate. All the scintigrams were obtained on a scintillation camera with high-resolution collimator in our clinic. Intracranial tumors were confirmed in 449 cases and 21 cases out of those were pineal tumors which were diagnosed by clinical symptoms, air study, angiography and Conray-or Myodil-ventriculography. In these pineal tumors, 14 (67%) out of the 21 cases had positive scan on scintigrams. All of our cases of teratoma (one case) and teratocarcinoma (two cases) showed clear abnormal uptake, though it had been reported that they do not tend to have positive results on scintigrams. We also performed scintigraphy on 11 cases out of the 21, both before and after 60Co radiation therapy. In the cases which showed either same grade or more increased abnormal uptake on scintigrams after radiation therapy, compared with that before radiation therapy, compared with that before radiation, their prognoses were poor. On the other hand, those cases which showed decreased abnormal uptake after radiation, have had a healthy daily activities. From these experiences, it may be concluded that brain scintigraphy is clinically valuable not only for making the diagnosis, but for evaluating the effect of radiation therapy and the prognosis in the cases of pineal tumor.

[The role of stimulation of the medullary reticular formation on intracranial pressure in cold injured brain].

This study was carried out to study the effect of stimulation of the reticular formation of the medulla oblongata on intracranial pressure (ICP) and cerebral blood volume (CBV) in injured brain with increased ICP. CBV was measured by the photoelectric method from the parietal lobe. Seventeen hours prior to the experiments, cold induced edema was produced to increase basal ICP. In 15 cats, electric stimulation produced temporary increases in BP, ICP and CBV and progressive intracranial hypertension was never observed (Group A). In 9 animals, progressive increases in CBV and ICP up to 50 to 100 mmHg were evoked after cessation of stimulation (Group B). Prestimulation ICP in Group B was significantly higher than that of Group A. Rapid and simultaneous increases in ICP and CBV following stimulation strongly suggested that global increments of CBV secondary to loss of cerebral vasomotor tonus were responsible for producing progressive intracranial hypertension. In Group B, the stimulation electrodes were invariably located at the area of the nucleus reticularis parvocellularis and gigantocellularis. Our experimental results show that in increased ICP a stimulated or irritable condition of the medullary reticular formation will cause acute progressive intracranial hypertension.

[A case of accessory nerve neurinoma presenting an intracisternal tumor].

A case of neurinoma from the spinal accessory nerve which is located in the cisterna magna is reported. A 54-year-old woman was admitted to the institute in 1990 with complaints of headache, nausea and ataxic gait for several months. Plain CT showed dilation of the lateral ventricles and a mass of lower density in the cisterna magna. The capsule and septa of the mass were enhanced with contrast medium. MRI showed the mass was low intense on T1-weighted images and high intense on T2-weighted images. Gadolinium visualized the mass multicystic. V-P shunt was performed before tumor resection. Through suboccipital craniectomy and C1 laminectomy the tumor was removed. The tumor had a long neck attached to the right spinal accessory nerve and extended to the cisterna magna.

[Unruptured cerebral aneurysms in two siblings screened by cerebral computed angiotomography].

The authors report two siblings, both of whom had unruptured cerebral aneurysms found by screening examination of noninvasive cerebral computed angiotomography. Other authors have reported unruptured cerebral aneurysms detected by conventional cerebral angiography in asymptomatic relatives of families in which two or more individuals had cerebral aneurysmal rupture. It is of interest that, in our cases, the unruptured cerebral aneurysms were detected by noninvasive cerebral computed angiography in two asymptomatic siblings in a family with no history of ruptured aneurysm. To the best of our knowledge, this is the first report of detection of unruptured familial aneurysm by cerebral computed angiotomography. Case 1 is a 67-year-old female who had been complaining of dullness in the head. Cerebral computed angiotomography showed a small high density nodule, suggesting an unruptured aneurysm of the right middle cerebral artery. An aneurysm with a diameter of 4 mm was found in the right middle cerebral artery. A 72-year-old male, who was a brother of case 1, had been afraid of having cerebrovascular disease, and wanted to have a neurological examination check-up. Computed angiotomography revealed a high-density nodule in the anterior communicating artery. Conventional cerebral angiogram showed a 6 X 7 mm aneurysm. However, both of the patients refused surgical treatment. Lozano et al reviewed the previously reported familial aneurysm cases. According to them, familial aneurysm tends to rupture at a younger age and at a smaller size than non-familial aneurysm. It is well known that asymptomatic members of familial aneurysm have a risk of developing aneurysm.(ABSTRACT TRUNCATED AT 250 WORDS)

[The effect of brain-stem vasomotor centers on the neurogenic control of cerebrovascular tonus--Part 3. The effects of destruction and stimulation of the brain-stem on intracranial pressure in acute subarachnoid hemorrhage].

The purpose of the present study is to clarify the effects of destruction and stimulation of the brain-stem on intracranial pressure (ICP) in experimentally induced subarachnoid hemorrhage (SAH). Using 23 cats, blood pressure (BP), ICP and local cerebral blood volume (CBV) were continuously measured. Acute SAH was produced by injection of autogenous blood (3 to 7 ml) into the cisterna magna. The animals were divided into two groups. Group A: those in which hypothalamic dorsomedial nucleus (DM) and reticular formation of the midbrain (MBRF) were coagulated bilaterally one hour after SAH and Group B: in addition to the procedure of Group A, reticular formation of the medulla oblongata (MORF) was electrically stimulated bilaterally. In 19 out of 23 cats of both groups, transient small increases in ICP and CBV were observed during coagulation and/or stimulation of DM, MBRF and MORF respectively in the animals whose ICP remained approximately 20 mmHg or below and progressive increase in ICP was never evoked. In 3 animals of Group A whose ICPs remained high at more than 20 mmHg, sequential destruction of DM and MBRF induced stepwise increase in ICP to 40 to 80 mmHg and consequently resulted in acute brain swelling. In 1 animal of Group B whose ICP fluctuated around 20 to 40 mmHg, biphasic increase in ICP to 100 mmHg was repeatedly evoked by stimulation of MORF. It is concluded that in the condition of increased ICP produced by SAH, lesions in the DM and MBRF and stimulating condition of MBRF may result in acute brain swelling.

[The role of brain-stem vasomotor centers on the neurogenic control of cerebrovascular tonus. Part 2: The effect of stimulation of the medullary reticular formation on cerebrovascular tonus].

Acute brain swelling has been proposed to be caused by vasomotor paralysis secondary to disruption of metabolic and/or neurogenic control of cerebrovascular tone. In previous experiments, acute brain swelling was produced by stimulation of the reticular formation of the medulla oblongata (MORF) with destruction of the dorsomedial nucleus of the hypothalamus (DM) and the reticular formation of the midbrain (MBRF) in 2 (out of 56) animals. The purpose of the present study is to clarify the effect of stimulation of the MORF on cerebrovascular tone. Using 32 cats, blood pressure (BP), intracranial pressure (ICP) and cerebral blood volume (CBV) were continuously measured. The animals were divided into 4 groups: those in which the ICP was normal (Group A), those in which the ICP increased after subarachnoid hemorrhage (Group B), those which underwent superior cervical ganglionectomy (Group C) and those in which the spinal cord was transected at the C2 level (Group D). In all animals, the MORF was stimulated after the DM and MBRF were destroyed. Thirty minutes after cessation of stimulation, the BP was increased again by injection of angiotensin II until it reached the same level as with MORF stimulation. The vasomotor index (VI), defined by delta ICP/delta BP, was calculated and compared between the two situations. BP, ICP and CBV increased simultaneously immediately after MORF stimulation. In 29 out of the 32 animals, ICP increased abruptly from 2 to 48 mmHg and after ten seconds or more decreased gradually. The BP rose about 50 mmHg more slowly than the ICP. After cessation of MORF stimulation, BP, ICP and CBV returned to the control value.(ABSTRACT TRUNCATED AT 250 WORDS)